I recently demonstrated attenuation of NaCl-induced hypertension in Dahl NaCl-sensitive (S) rats by supplementing calcium (Ca) in the diet. Three observations indicated that this attenuation was mediated by neural not vascular mechanisms. 1) Difference in arterial pressure between awake S rats on high vs normal Ca diet was abolished by ganglionic blockade. 2) Baroreflex control was significantly augmented by high Ca diet. 3) After ganglionic blockade pressor responses to adrenergic and nonadrenergic vasoactive agents were similar between groups. High calcium intake also normalized plasma Ca (total) and phosphorus concentrations which were clearly below and above reported normal values, respectively, without Ca supplementation. My overall goal is to identify mechanisms by which high Ca diet attenuates neural contribution to hypertension in Dahl S rats. First, vasoconstrictor responses to sympathetic nerve stimulation, but not to norepinephrine (NE), are enhanced by high NaCl diet in Dahl S rats. Thus, local neural NE release appears to be facilitated by high NaCl intake in S rats. I will determine if high Ca intake corrects this neural alteration and if such correction is dependent on normalization of plasma phosphorus or associated with prevention of hypocalcemia in S rats. Second, baroreflexes are impaired in prehypertensive Dahl S rats. My recent work showed that high Ca intake augmented baroreflex function in hypertensive S rats fed high NaCl. This could reflect a direct action of long-term high Ca feeding on baroreceptor function or a secondary effect of attenuation of the NaCl-induced hypertension. I will determine if high Ca intake restores normal baroreflex function in prehypertensive S rat with no NaCL- induced hypertension. Third, I have also shown that basal sympathetic tone as indexed by NE turnover is higher in selective regions of awake, resting Dahl S rats than in R rats fed high NaCl. Differences in central NE turnovers were also observed. I will determine if high calcium intake attenuates increased peripheral NE turnovers and reverses alterations in central NE turnovers in awake Dahl S vs R rats on high NaCl diet. In summary, I will determine which of these different indices of neural dysfunction in S rats are normalized by high calcium intake. In addition, I will test the hypothesis that high NaCl intake induces um intake. In addition, I will test the hypothesis that high NaCl intake induces ionic and hormonal hypocalcemia in Dahl S but not R rats, a condition which may contribute to their neurogenic hypertension and may be normalized by high Ca ingestion.